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Pharm Year 3 Sem1 patient > gluacoma > Flashcards

gluacoma Flashcards

1
Q

what is glaucoma?

A

blanket term for a variety of conditions

• Common factor is acquired progressive neuropathy (if untreated)
• Optic nerve damage
• Visual field loss
Eventual blindness

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2
Q

what are the risk factors of glaucoma?

A 
• Normally asymptomatic
• High IOP (>21mmHg)
• Family history of glaucoma
• Race - afro Caribbean 
• Systemic hypertension
• Cardiovascular disease
• Migraine
Previous ocular disease
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3
Q

what are the main aims of a glaucoma treatment?

A
  • Reduce IOP
    • <16-20mmHg depending on patient
  • Drug to have sufficient duration of action (esp eyedrops)
    • Patient compliance
  • Provides:
    • Preservation of visual field
    • No loss of effect over time
    • Compatibility with other treatments
    • No topical or systemic side effects
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4
Q

what drugs are used to treat glaucoma?

A

prostaglandins and prostamide analogues

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5
Q

what types of gluacoma are there?

A

primary and secondary
open angle

close angle

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6
Q

what are the symptoms of glaucoma

A

asymptomatic

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7
Q

describe the aetiology of glaucoma

A

impaired drainage of aqueous humour

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8
Q

how is closed angle glaucoma treated

A

surgery

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9
Q

how is aqueous humour produced?

A 
large blood supply
fluid from capillaries
into epithelial cells makes humour
comes round the lens
comes out of the pupil
into the side
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10
Q

describe the main parts of the eye?

A

iris, pupil, lens, colliery muscle

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11
Q

where is aqueous humour produced?

A

outermost cells - epithelial cells of the eye

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12
Q

open angle

A

angle between the iris and the sclera

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13
Q

trabecular meshwork

A

aq humour flows through space cells into the collector channel and out the episcleral vein
because pressure in episceral vein is lower
8mmHg to 16mmHg

80% fluid through

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14
Q

uveoscleral outflow

A

20% flow

bypass trabecular meshwork
sclera ancillary body
more resistance as there is much less space for fluid to move
goes through much slower

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15
Q

Prostaglandins

A

PGE required for production of aq humour but not stable
PG f2alpha more stable

latanoprost, tafluprost and travoprost
(esters)

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16
Q

prostamides analogues?

A

bimatoprost

prostamide f2alpha precursor

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17
Q

why use prostaglandins analogues?

A

produced naturally in most cells
involved in aq humour outflow

1st choice clinically: uniquely decrease IOP , most effective

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18
Q

how do prostaglandin analogues work ?

A

act on the PG2Falpha receptor
ester converted back to acid (by esterase’s in the eye)
GPCR (g alpha q)

activates PLC, DAG, IP3

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19
Q

which glaucoma drugs act by increasing aqueous outflow?

A

prostaglandin analogues - increase uveoscleral outflow
praostamide analogues - inc trabecular outflow
parasympamimetic drugs - inc trabecular outflow

20
Q

which glaucoma drugs act by decreasing aqueous humour production ?

A

beta blockers -

alpha selective -

21
Q

name the parasympathomimetic drugs?

A

pilocarpine

22
Q

where are Fp receptors found?

A

• Ciliary body & muscle, sclera (mainly)
• Iris sphincter (small amounts)
Trabecular meshwork cells (few present)

23
Q

advantages of prostaglandin analogues and prostamide analogues

A

once a day (night)
good tolerability
Efficacious
reduce IOP by 35%

24
Q

describe the main action of prostamide analogues

A

increases both trabecular outflow and uveoscleral outflow via binding to F2a receptors and prostamide receptors

25
describe the main action of prostaglandin analogues
reduced resistance to uveoscleral outflow by remodelling extracellular matrix : inc matrix metalloproteinases decreases collagen and extracellular matrix decreases resistance of colliery muscle and sclera to increase outflow most likely via FP receptors -
26
side effects of prostaglandin analogues
red eye inc pigmentation of iris, eyelash and periocular skin, eyelash growth precipitate or worsen cystoid macular oedema in aphasic eyes sensitivity to light contraindicated in pregnancy - can induce labour and affect cell division
27
how are beta blockers used to treat glaucoma ?
decrease aqueous humour production by block beta receptors , inhibiting cAMP production NA+K+2Cl- co-transoporter activation and Cl- efflux don't occur decreased ion transport decreases aq humour production as osmotic gradient not present
28
advantages of beta blockers
rapid onset well tolerated 20-30 % reduction compatible with other drugs
29
Disadvantages of beta blockers
more easily absorbed systemically systemic side effects efficacy declines over time twice daily admin or once daily with certain preparations
30
side effects of beta blockers
generally systemic cardiovascular - bradycardia,hypotension,peripheral,vasoconstriction,impotence, C/I in heart block,failure bronchial : constriction of bronchioles : c/I in asthma and COPD diabetes: block sympathetic response - mask hypo
31
advantages of fixed dose combination
``` different classes of drugs - additive effects patient compliance reduced exposure to preservatives avoid washout effect of 2nd drop decrease treatment dose decrease patient cost - 1 Rx charge ```
32
describe treatment pathway for glaucoma
Prostaglandin/prostamide analogues analogues beta blockers fixed combination carbonic anhydrase inhibitor
33
how do carbonic anhydrases inhibitors work?
inhibit carbonic anhydrases in cilliery epithilium - reduced ion gradient - reduced aq humour production
34
name a systemic CAI | how and when are systemic CAIs used?
drug: acetozolamide not absorbed topically, not v lipophilic when IOP is very elevated/ emergency injected used in OAG,secondary glaucoma, per iteratively in acute angle closure glaucoma
35
acetazolamide side effects
sulfanimde derivative - allergies and blood disorders enzymes across the body : GI effects, diuresis, drowsiness, acid/base imbalance depression parasthesias
36
how can acetazolamide be adapted for ocular use? How does this change the drug? give examples
modify to giver better lips solubility decreasing side effects more selective for CA-II enzyme Dorzolamide and brinzolamide
37
describe the effects of topical CAIs. When are they used
20% IOP reduction adjunct therapy or single therapy if beta blockers not indicated local side effects
38
describe side effects of topical CAIs
transient burning, stinging pH brinzolamide drops (7.5,5.6-6.0) blurred vision conjunctival hyperaemia transient myopia, blepharitis, allergic conjunctivitis taste disturbances, dry mouth, headache
39
describe mechanism of action for alpha2 adrenoreceptor agonists
alpha receptor selective receptors are on the ciliary, conjunctival and corneal epithelial cells decrease aq secretion by decreasing cAMP - decrease ion transport- decrease aq secretion decreases ultrafiltration inc uveosceral outflow
40
advantages of a2 adrenoreceptor agonists
no mydriasis no vasoconstriction little effect on CV system
41
why can a2 adrenorecptor agonists be considered neuroprotective?
preserve optic nerve and retinal ganglion cells
42
give an example of a2 adrenorecptor drugs | briefly describe their characteristics
brimonidine - selective rapid 2hr onset apraclonidine - less selective, short term use (causes tachy) used post laser eye surgery to prevent IOP rise
43
a2 adrenorecptor agonist side effets
local - allergy, sting, burn ,blurred vision, photophobia | systemic - hypotension
44
mechanism of parasympathomimetic drugs?
``` m3 receptor agonists contract ciliary muscle pull scleral spur opens trabecular meshwork inc trabecular outflow decrease IOP ``` last 6hr cyclical effect on IOP through day QDS patient compliance reduced
45
parathesiais
burning tingling of skin - experienced with carbonic anhydrases

Pharm Year 3 Sem1 patient (12 decks)

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